Central effect of angiotensin III on caudal hypoglossal neurons in rats

We communicated the central effect of angiotensin III (ANG III), a potent signal for extracellular dehydration, on single neurons in the caudal hypoglossal nucleus of Sprague-Dawley rats anesthetized with pentobarbital sodium. A significant number (121 of 168) of caudal hypoglossal neurons responded to intracerebroventricular application of ANG III (80 or 160 pmol), with either an increase (n = 83) or decrease (n = 38) in their spontaneous discharge. These effects of ANG III were significantly reversed by intracerebroventricular application of the nonpeptide angiotensin AT1 receptor antagonist losartan (40 nmol), but not by the AT2 antagonist, PD-123319. The hypoglossal neuronal responses to repeated administration of ANG III (80 pmol), delivered at an interval < or = 18 min, exhibited acute tachyphylaxis. Intracerebroventricular administration of the cholinergic dipsogen, carbachol (50 ng), or the osmotic stimulant, hypertonic saline (0.5 M), also elicited responses in ANG III-responsive hypoglossal neurons. These results suggest that neurons in the caudal hypoglossal nucleus may serve as the final common pathway for extracellular and, possibly, intracellular thirst in the rat. Furthermore, it is likely that the action of ANG III is mediated by the AT1 subtype of angiotensin receptors.